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Substance Abuse and Posttraumatic Stress Disorder Author(s): Kathleen T. Brady, Sudie E. Back and Scott F. Coffey Source: Current Directions in Psychological Science, Vol. 13, No. 5 (Oct., 2004), pp. 206-209 Published by: Sage Publications, Inc. on behalf of Association for Psychological Science Stable URL: http://www.jstor.org/stable/20182954 Accessed: 27-11-2016 20:00 UTC

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CURRENT DIRECTIONS IN PSYCHOLOGICAL SCIENCE

Substance Abuse and Posttraumatic Stress Disorder

Kathleen T. Brady, Sudie E. Back, and Scott F. Coffey

Medical University of South Carolina and University at Buffalo, State University of New York

ABSTRACT?Posttraumatic stress disorder (PTSD) and substance use disorders (SUDs) frequently co-occur. Among individuals seeking treatment for SUDs, approximately 36% to 50% meet criteria for lifetime PTSD. The self-medication and suscepti bility hypotheses are two of the hypotheses that have been proposed to help explain the etiological relationship between PTSD and SUDs. It is also possible that common factors, such as genetic, neurobiological, or environmental factors, contribute to the high rate of PTSD-SUD co-occurrence. Preliminary results

from integrated psychotherapy approaches for the treatment of patients with both disorders show promise. This article reviews these and other advances in the study of comorbid PTSD and SUDs, and suggests areas for future work.

KEYWORDS?posttraumatic stress disorder; trauma; substance use disorders; addiction; comorbidity

Posttraumatic stress disorder (PTSD) is characterized by symptoms that persist for at least 1 month following exposure to a traumatic event. Interpersonal violence (e.g., physical and sexual abuse), com bat, and natural disasters are examples of traumas commonly asso ciated with PTSD. The characteristic symptoms of PTSD can be divided into three clusters: avoidant, intrusive, and arousal symptoms.

Examples of intrusive symptoms include unwanted thoughts or flashbacks of the event. Avoidant symptoms include, for example, attempts to avoid any thoughts or stimuli that remind one of the event.

These symptoms are particularly relevant to this review because substances of abuse are often used by individuals with PTSD in an attempt to avoid or escape memories. Arousal symptoms generally include exaggerated startle reflex, sleep disturbance, and irritability,

and are generally associated with hyperactivity of the autonomie nervous system. These symptoms are also pertinent to our discussion here because the use and withdrawal of many substances of abuse are

associated with autonomie nervous system hyperactivity.

A number of recent studies have emphasized the common co-oc currence (i.e., comorbidity) of PTSD and substance use disorders (SUDs). The interaction between PTSD and SUDs is likely multifac eted and variable. Further exploration of the relationship between these two disorders may prove useful in explicating the underlying

pathophysiological processes involved. In this article, we explore the

relationship between PTSD and SUDs.

PREVALENCE

The prevalence of the co-occurrence of PTSD and SUDs has been examined in epidemiological studies in the general population, as well as in studies of individuals who seek treatment for one or both of these

disorders.

Epidemiological Studies Epidemiological investigations provide information about the number

of individuals with a given disorder in the general population or in subgroups of the general population. Two large epidemiological studies focusing on psychiatric disorders have been conducted fairly

recently in the United States: the Epidemiologie Catchment Area Study (ECA; Regier et al., 1990) and the National Comorbidity Study (NCS; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995).

The ECA data revealed that men with PTSD were 5 times as likely and women with PTSD were 1.4 times as likely to have drug abuse or dependence, compared with individuals without PTSD. Using the ECA data, Cottier, Compton, Mager, Spitznagel, and Janea (1992) found that cocaine and opiate users had the highest rate of PTSD, which was 10 times higher than the rate in other SUD groups.

In the NCS sample, approximately 7.8% of the participants (5.0% of men, 10.4% of women) met criteria for lifetime PTSD (i.e., were diagnosed with PTSD at some point in their lifetime), and 35.4% of men and 17.9% of women met criteria for an SUD. More than half

(51.9%) of men and 27.9% of women with PTSD met criteria for lifetime alcohol abuse or dependence.

Studies of Individuals Seeking Treatment Studies of individuals seeking treatment for SUDs indicate an ex traordinarily high prevalence of PTSD in this group. In a number of

studies examining individuals with drug or alcohol use disorders, the lifetime prevalence of PTSD was found to be between 36% and 50%, and the current prevalence of PTSD was between 25% and 42% (Jacobsen, Southwick, & Kosten, 2001). The wide variability in these numbers reflects the differing populations and diagnostic techniques used in different studies. In general, PTSD is more common in women with SUDs than in men with SUDs.

Address correspondence to Kathleen T. Brady, Medical University of South Carolina, Division of Clinical Neuroscience, 67 President St., P.O. Box 250861, Charleston, SC 29425; e-mail: [email protected].

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Kathleen T. Brady, Sudie E. Back, and Scott F. Coffey

The most common types of traumas reported among individuals with

PTSD and SUDs are interpersonal, usually involving sexual abuse among women and physical abuse or assault among men. Patients in

treatment for PTSD and SUDs also frequently report childhood his tories of emotional and physical neglect or abuse, rape or sexual as sault, witnessing domestic violence, robbery, death of a loved one due

to homicide, and unhealthy environments. It is important to note that

most individuals with both PTSD and an SUD report experiencing multiple traumatic events during their lifetimes.

ETIOLOGICAL RELATIONSHIPS BETWEEN PTSD AND SUDS

Although PTSD and SUDs appear to be strongly linked, little is known

about the nature of their relationship. The most widely held expla nation of their frequent co-occurrence is the self-medication hypoth

esis. This hypothesis is based primarily on clinical observation and posits that traumatized individuals attempt to use substances in order

to dampen traumatic memories, or to avoid or "escape" from other

painful symptoms of PTSD. A second hypothesis, the high-risk hy pothesis, posits that individuals with SUDs, because of high-risk lifestyles, are likely to experience a trauma and are, therefore, more

likely than the general population to develop PTSD. Finally, a third hypothesis, known as the susceptibility hypothesis, states that sub

stance use increases an individual's susceptibility to developing PTSD following a trauma.

Chilcoat and Breslau (1998) have tested these three hypotheses using a large longitudinal data set drawn from a health maintenance

organization. The authors found that having PTSD greatly increased the risk of developing a subsequent SUD, but exposure to a traumatic event that did not result in PTSD did not increase the risk of devel

oping a subsequent SUD. Thus, it appears to be the development of PTSD, not exposure to trauma per se, that increases the risk of de

veloping an SUD. In addition, the study found that drug abuse or dependence did not increase, or only slightly increased, an individ ual's risk of developing PTSD, and did not increase an individual's risk of trauma exposure. The findings from Chilcoat and Breslau's

study provide strong support for the self-medication hypothesis and

little support for the high-risk hypothesis.

Another possible explanation for the high comorbidity of PTSD and SUDs is that the disorders have common susceptibility factors. These might be genetic, neurobiological, or environmental. To date, studies that have examined family patterns of the two disorders do not support

the hypothesis that there is a genetic vulnerability common to PTSD and SUDs (S.H. Stewart & Conrod, 2003).

Although a full description of the commonalities in neurobiology between PTSD and SUDs is beyond the scope of this report, there is

growing evidence that shared neurobiological relationships may play a

significant role in PTSD-SUD comorbidity. In a description of fear conditioning, Armony and LeDoux (1997) proposed that information about a traumatic event is sent to the amygdala via the sensory thal

amus or indirectly via the cortex or the hippocampus (a structure important for memory and spatial perception). The activation of the

central nucleus of the amygdala causes a fear response, followed by

activation causing an anxiety response. Interestingly, a number of abused drugs exert their anxiety-reducing effects by inhibiting activity

in the amygdala, and this inhibition leads to an attenuated startle response (recall that an exaggerated startle response is one of the

symptoms of PTSD). Alcohol may also inhibit the startle response by acting on the amygdala and the cortex. The areas activated by fear and

anxiety associated with PTSD may be inhibited by drugs of abuse, so

neurobiological evidence supports the self-medication hypothesis.

Other investigations have focused on the hypothalamic-pituitary adrenal (HPA) axis, the primary neuroendocrine system involved in the stress response (J. Stewart, 2003). Abnormalities in the function of

the HPA axis have been implicated in both PTSD and SUDs. Animal studies have demonstrated that exposure to stress facilitates both the

initiation of substance use and its reinstatement after a period of abstinence in previously dependent animals (Kreek & Koob, 1998). This reinstatement can be blocked by drugs that interfere with the

activity of the HPA axis (Kreek & Koob, 1998; J. Stewart, 2003). The "fight or flight" (noradrenergic) system is also intimately involved in

the stress response. Increased activity in the noradrenergic system leads to the increase in blood pressure, heart rate, and sweating often

seen with the fear response. This system is activated during with drawal from many substances of abuse, providing another potential neurobiological link between PTSD and SUD.

TREATMENT

The treatment of individuals with co-occurring PTSD and SUDs has only recently been explored systematically. Therefore, most of the data

in this area are preliminary, but there are a number of promising approaches under development.

Psychotherapy The psychotherapeutic treatment of comorbid PTSD and substance use has received much recent attention. In the past, individuals with PTSD and SUDs received treatment for their substance use, and

treatment of PTSD was deferred. More recently, this approach has been considered problematic because the symptoms of PTSD (i.e., sleep disturbance and intrusive thoughts) may drive relapse to sub stance use. In response to this concern, integrated therapies targeting both disorders have been developed and are under investigation (Ouimette & Brown, 2003). Most of these therapies combine suc cessful elements of existing psychotherapeutic treatments for sub stance abuse and trauma. For both disorders, cognitive-behavioral strategies, in particular, have demonstrated success. Several prelim inary studies support the use of the Seeking Safety (SS) program. This

is a manual-guided group therapy designed specifically for women with PTSD and substance dependence and consists of 25 sessions equally aimed at modifying thoughts, behaviors, and interpersonal issues (Najavits, Weiss, Shaw, & Muenz, 1998). In one controlled trial,

SS and relapse prevention therapy (another cognitive-behavioral therapy, in this case aimed at preventing return to substance use) were equally efficacious, and both were superior to treatment as usual

The amygdala and thalamus are part of the limbic system, which plays a critical role in processing emotional information. The thalamus computes both nonemotional and emotional information and then sends this information on to

the amygdala. The amygdala is central to the expression of negative emotions in humans and has been associated with anger, avoidance, and fear.

The HPA axis helps to regulate the body's stress symptoms. It controls the release of stress hormones and aids in reestablishing a steady state after a disturbance or stressful event.

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Substance Abuse and Posttraumatic Stress Disorder

(i.e., standard treatment they would receive in a clinic if they were not

participating in a research study). One controversy concerning integrated psychotherapy involves the

use of exposure-based PTSD therapy in substance-dependent indi viduals. There is a great deal of empirical evidence supporting ex posure-based treatment for PTSD, which involves helping patients confront memories, places, or specific situations that remind them of

the trauma, that they have avoided, and that now evoke unrealistic and

intense fear (Friedman, Davidson, Mellman, & Southwick, 2000). This

therapy can cause distress and discomfort and was not recommended for individuals with SUDs because of the concern that exposure might

precipitate relapse in this vulnerable population. However, several recent studies have demonstrated successful use of exposure-based therapy in some individuals with co-morbid PTSD and SUDs, although

the sample sizes of these studies were small and dropout rates high (Back, Dansky, Carroll, Foa, & Brady, 2001; Coffey, Dansky, & Brady,

2003; Triffleman, Carroll, & Kellogg, 1999). Although the early results from integrated treatments suggest that

they may be helpful for many individuals with PTSD and SUDs, the studies of these treatments have been limited by small sample sizes,

lack of comparison groups, and high dropout rates. To date, only one

controlled trial using integrated psychotherapies has been conducted.

Thus, it is not yet known whether integrated treatments are superior to

sequential therapies (i.e., treating one disorder and then the other) or

single-model therapies (i.e., treating only one of the disorders), how the various integrated treatments compare with one another, who benefits most from integrated treatments, and for whom integrated treatments are contraindicated.

Pharmacotherapy One important goal of pharmacotherapy for comorbid PTSD-SUDs is to reduce key symptoms of PTSD so that patients do not need to use substances of abuse to distance themselves from the traumatic event.

In early double-blind, placebo-controlled studies, tricyclic and monoamine-oxidase inhibitor antidepressants (e.g., Elavil, Pamelor, Nardil) were shown to improve intrusive and depressive symptoms of PTSD. There have also been uncontrolled trials suggesting positive effects of other medications, including carbamazepine, beta-blockers,

clonidine, benzodiazepines, and lithium. More recently, a number of placebo-controlled trials with relatively large numbers of subjects have demonstrated that serotonin-reuptake inhibitors, specifically, sertraline (i.e., Zoloft), fluoxetine (i.e., Prozac), and paroxetine (i.e., Paxil), are useful in treating PTSD (Friedman et al., 2000). In addi tion, pharmacotherapeutic treatments for SUDs may prove useful among individuals with comorbid PTSD. Although there have been no

controlled trials of such approaches, recent advances in psychother apeutic treatment for alcohol, opiate, and nicotine dependence suggest

new possibilities. This is clearly an area that warrants investigation.

CONCLUSIONS AND FUTURE DIRECTIONS

Although there has been a great deal of recent study focused on the relationships among stress, PTSD, and SUDs, much work remains. Further investigation of the neurobiological interface between PTSD and SUDs is needed to provide more information about the mecha nisms underlying their causal connection. The noradrenergic system and HPA axis are two systems that are implicated in the pathophys

iology of both SUDs and PTSD. Does chronic use of cocaine, alcohol, and other substances of abuse lead to changes in the noradrenergic, HPA, or other systems that make an individual more susceptible to the

development of PTSD? Conversely, does a traumatic experience, particularly childhood trauma, lead to changes in neurotransmitter and neuroendocrine systems that make an individual more vulnerable

to the development of an SUD? Additional treatment studies are also critically important. The

commonalities in the pathophysiology of PTSD and SUDs suggest that

pharmacotherapies targeting specific neurotransmitter or neuroendo

crine systems might be particularly beneficial, yet there has been little

exploration of agents that act on either the noradrenergic system or the HPA axis in individuals with both disorders.

Although there have been promising developments in psychother apeutic treatments, the question of the safety and efficacy of exposure

based treatment for PTSD in substance-using populations still remains

unanswered. It seems likely from the data obtained thus far that ex

posure-based treatment may be beneficial for a subset of patients. Further exploration of different types and timing of psychotherapeutic

interventions will be important. Finally, how to integrate pharmaco

therapeutic and psychotherapeutic treatments to maximize outcomes

is of critical importance. In particular, would medications be useful in

early stages of recovery to help patients engage in and comply with psychotherapy, or are medications better utilized for patients who do

not respond to psychotherapeutic interventions alone?

In conclusion, further exploration of PTSD, substance use, and the

connections between these two disorders could provide information that will help not only in the treatment of these disorders, but also in

the broader understanding of the complexity of the relationship be tween external Stressors and the development of psychopathology.

Recommended Reading Chilcoat, H.D., & Breslau, N. (1998). (See References)

Jacobsen, L.K., Southwick, S.M., & Kosten, T.R. (2001). (See References)

Kreek, M., & Koob, G. (1998). (See References)

Ouimette, P., & Brown, P.J. (Eds.). (2003). (See References)

Stewart, J. (2003). (See References)

REFERENCES

Armony, J.L., & LeDoux, J.E. (1997). How the brain processes emotional in formation. In R. Yehuda & A.C. McFarlane (Eds.), Psychobiology of posttraumatic stress disorder (pp. 259-270). New York: New York Acad emy of Sciences.

Back, S.E., Dansky, B.S., Carroll, K.M., Foa, E.B., & Brady, K.T. (2001). Ex posure therapy in the treatment of PTSD among cocaine-dependent in dividuals: Description of procedures. Journal of Substance Abuse Treatment, 21, 35-45.

Chilcoat, H.D., & Breslau, N. (1998). Investigations of causal pathways be tween PTSD and drug use disorders. Addictive Behaviors, 23, 827-840.

Coffey, S.F., Dansky, B.S., & Brady, K.T. (2003). Exposure-based trauma-fo cused therapy for comorbid posttraumatic stress disorder-substance use disorder. In P. Ouimette & P.J. Brown (Eds.), Trauma and substance abuse: Causes, consequences, and treatment of comorbid disorders (pp. 127-146). Washington, DC: American Psychological Association.

Cottier, L., Compton, W., Mager, D., Spitznagel, E., & Janea, A. (1992). Posttraumatic stress disorder among substance users from the general population. American Journal of Psychiatry, 149, 664-670.

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Kathleen T. Brady, Sudie E. Back, and Scott F. Coffey

Friedman, M.J., Davidson, J.R.T., Mellman, T.A., & Southwick, S.M. (2000). Pharmacotherapy. In E.B. Foa, T.M. Keane, & MJ. Friedman (Eds.), Effective treatments for PTSD: Practice guidelines from the International Society for Traumatic Stress Studies (pp. 84-105). New York: Guilford Press.

Jacobsen, L.K., Southwick, S.M., & Kosten, T.R. (2001). Substance use dis orders in patients with posttraumatic stress disorder: A review of the literature. American Journal of Psychiatry, 158, 1184-1190.

Kessler, R.C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C.B. (1995). Posttraumatic stress disorder in the National Comorbidity Survey. Ar chives of General Psychiatry, 52, 1048-1060.

Kreek, M., & Koob, G. (1998). Drug dependence: Stress and dysregula tion of brain reward pathways. Drug and Alcohol Dependence, 51, 23-47.

Najavits, L.M., Weiss, R.D., Shaw, S.R., & Muenz, L.R. (1998). "Seeking Safety": Outcome of a new cognitive-behavioral psychotherapy for women with posttraumatic stress disorder and substance dependence. Journal of Traumatic Stress, 11, 437-456.

Ouimette, P., & Brown, PJ. (Eds.). (2003). Trauma and substance abuse: Causes, consequences, and treatment of comorbid disorders. Washington, DC: American Psychological Association.

Regier, D.A., Farmer, M.E., Rae, D.S., Locke, B.Z., Keith, S.J., & Judd, L.L. (1990). Comorbidity of mental disorders with alcohol and other drug abuse: Results from the Epidemiologie Catchment Area (ECA) Study. Journal of the American Medical Association, 264, 2511-2518.

Stewart, J. (2003). Stress and relapse to drug seeking: Studies in laboratory animals shed light on mechanisms and sources of long-term vulnerability. American Journal on Addictions, 12, 1?17.

Stewart, S.H., & Conrod, PJ. (2003). Psychosocial models of functional asso ciations between posttraumatic stress disorder and substance use disor ders. In P. Ouimette & PJ. Brown (Eds.), Trauma and substance abuse: Causes, consequences, and treatment of comorbid disorders (pp. 29-55). Washington, DC: American Psychological Association.

Triffleman, E., Carroll, K, & Kellogg, S. (1999). Substance dependence posttraumatic stress disorder therapy: An integrated cognitive-behavioral approach. Journal of Substance Abuse Treatment, 17, 3-14.

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